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Haematology > Leukaemia > Flashcards

Leukaemia Flashcards

1
Q

What is leukaemia?

What is the difference between chronic and acute leukaemias?

A

Cancer of haemopoietic stem cells which leads to unregulated production of certain types of blood cells

Chronic= slowly progressing and occurs further down differentiation path

Acute= fast progressing transformation of haemopoietic stem cells

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2
Q

What are the 4 main types of leukaemia?

A

Acute myeloid leukaemia

Acute lymphoblastic leukaemia

Chronic myeloid leukaemia

Chronic lymphocytic leukaemia

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3
Q

What is the underlying pathophysiology of leukaemias?

What charactertic features does this result in?

A

Genetic mutation in precusor leads to excessive production of white cell type

Features:
Leucocytosis= due to excessive WBC 
Pancytopenia:
-anaemia 
-leukopenia 
-thrombocytopenia

Due to excess production of one cell type creating space occupying lesion in bone marrow and ultimately leading to bone marrow failure

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4
Q

What happens to malignant leukocytes in the CML and CLL?

What might patients present with as a result?

A

Leukocytes ACCUMULATE

CML:
-splenomegaly

CLL:

  • splenomegaly
  • hepatomegaly
  • lymphadenopathy
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5
Q

What are the different ages of presentation for the different forms of leukaemia?

A

Way to remember:
ALL CeLLmates have CoMmon AMbitions
With each type of leukaemia progression by 10 years between 45-75

ALL= <5 + >45 years 
CLL= >55
CML= >65
AML= >75
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6
Q

How might someone with leukaemia present?

A 
(Non-specific presentation) 
Fatigue 
Fever 
Failure to thrive (children)
Pallor secondary to anaemia 
Petechiae + abnormal bruising 
Abnormal bleeding 
Lymphadenopathy (CLL)
Hepatosplenomegaly (CLL)
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7
Q

What other differentials should be considered for petechiae?

A

Menigoccocal septicaemia

Vasculitis

Henoch-schonlein purpura

ITP

Non-accidental injury-> ABUSE.

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8
Q

What investigations are done if leukaemia is suspected?

A

FBC
-w/i 48 hrs if patient suspected of leukaemia

Blood film
-abnormal cells

LDH
-can be raised in leukaemia but is not specific

Bone marrow biopsy
-establishes definitive diagnosis of leukaemia

CXR

  • infection
  • mediastinal lymphadenopathy

Lumbar puncture
-when suspecting that CNS is involved

CT/MRI/PET
-staging

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9
Q

What are the different bone marrow samples which can be taken to aid diagnosis of leukaemia?

A

Bone marrow aspiration

  • liquid sample of cells
  • architecture not maintained

Bone narrow trephine

  • solid core sample of bone marrow
  • architecture maintain

Bone marrow biopsy

  • taken from iliac crest
  • can be examined straight away whereas need to way few days for trephine samples
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10
Q

What is acute promyelocytic leukaemia?
What cause APL?
How can it be treated?

A

Subtype of AML where differentiation of myeloblasts is halted at promyelocyte stage

  • leads to loss of neutrophil production
  • immature promyelocytes accumulate in the bone marrow and eventually leak into blood

Fusion protein (PML-RARA) due to reciprocal translocation of chromosome 15/17= causes the arrest at promyelocyte stage

Vesanoid + Arsenic trioxide
-leads to degradation of fusion protein (PML-RARA) which lifts the block in differentiation

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11
Q

What are important features of AML?

What would a blood film show?

A

Many different types with slight cytogenic differences
Most common acute leukaemia in adults
Typically presents in middle age
Can occur due to transformation from myeloproliferative disease

High proportion of blast cells
-blast cells have rods in cytoplasma called Auer rods

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12
Q

What is the characteristic cause of CML?

A

Translocation between chromosome 9 and chromosome 22 to form Philidelphia chromosome i.e. BCR-ABL oncogenic fusion protein
-BCR-ABL has constituitive tyrosine kinase activity leading to promotion, proliferation and survival of leukocytes

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13
Q

What are the 3 typical phases of CML?

A

Chronic:

  • can last for 5 years
  • often asymptomatic I.e. patients diagnosed incidentally with raised WCC

Accelerated phase:

  • blast cells take up high proportion of bone marrow and blood
  • patients become symptomatic i.e. anaemia/thrombocytopenia/immunocompromised

Blast phase

  • higher proportion of blast cells in blood and BM
  • severe symptoms + pancytopenia
  • often fatal
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14
Q

What targetted treatment can be used in CML?

What is the potential problem with this treatment?

A

Tyrosine kinase inhibitors to inhibit the acitivity of BCR-ABL fusion protein i.e. Imatinib

CML can develop resistance

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15
Q

What occurs in chronic lymphocytic leukaemia?
How might someone with CLL present?
What might a blood film show?

A

Chronic proliferation of well-differentiated lymphocyte i.e. commonly B lymphocytes

>55 
Asymptomatic
Infections 
Anaemia 
-warm AI haemolytic anaemia 
Bleeding 
Weightloss
Can present with B symptoms 
Hepatomegaly
Lymphadenopathy= due to CLL cells proliferating in w/i centres of LN

I.e. signs of bone marrow failure

Smear/smudge cells
-occurs when blood sample being prepared due to WBC being fragile and rupturing creating a smudge

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16
Q

What is the pathobiology underlying CLL?

A

B-cell proliferation pathway targeted
CLL express BCL-2 i.e. anti-apototic proteins

Therefore= combination of proliferation and resistance to apoptosis which drives the increased production of B lymphocytes

NOTE: no single lesion-> can be quite heterogenous

17
Q

What is Richter’s transformation?

A

Where CLL transforms into high grade lymphoma

18
Q

What are the possible treatment options for CLL?

Can it be cured?

A

Targeted therapy

  • Bcl-2 inhibitors
  • BCR signallying inhibitors= leads to blockage of key interactions needed for proliferation

Chemoimmunotherapy

MAb

Chemo

19
Q

What occurs in acute lymphoblastic leukaemia?

How is most commonly affected by ALL?

A

Malignant change in lymphocytic precusor cell leading to acute proliferation of single lymphocyte= usually BC

Leads to pancytopenia due to excessive proliferation causing them to occupy majority of BM and meaning there is not space for proliferation of other cell types

Most common cancer in children -> peak between 2-4 years
Can affect adults >45
Associated with Downs syndrome

20
Q

What is the general management principles for leukaemia?

A

Chemotherapy + steroids= main stay

Others:
Radiotherapy
Target therapy 
Biological therapy 
BM transplant 
Surgery
21
Q

What are possible complications of chemotherapy?

How is tumour lysis syndrome associated with chemotherapy?

A

Stunted growth and development when used in children i.e. ALL

Infections -> has immunosuppressive effects

Neurotoxicity

Infertility

Secondary malginancy

Cardiotoxicity

Tumour lysis syndrome:

  • release of uric acid from cells which have been destroyed by chemo
  • can lead to uric acid forming crystals in kidney leading to AKI
  • need to give allopurinol

Haematology (17 decks)

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